"There's a little bit of mistrust": Red River Métis experiences of the H1N1 and COVID-19 pandemics.

We examined the perspectives of the Red River Métis citizens in Manitoba, Canada, during the H1N1 and COVID-19 pandemics and how they interpreted the communication of government/health authorities' risk management decisions. For Indigenous populations, pandemic response strategies play out within the context of ongoing colonial relationships with government institutions characterized by significant distrust. A crucial difference between the two pandemics was that the Métis in Manitoba were prioritized for early vaccine access during H1N1 but not for COVID-19. Data collection involved 17 focus groups with Métis citizens following the H1N1 outbreak and 17 focus groups during the COVID-19 pandemic. Métis prioritization during H1N1 was met with some apprehension and fear that Indigenous Peoples were vaccine-safety test subjects before population-wide distribution occurred. By contrast, as one of Canada's three recognized Indigenous nations, the non-prioritization of the Métis during COVID-19 was viewed as an egregious sign of disrespect and indifference. Our research demonstrates that both reactions were situated within claims that the government does not care about the Métis, referencing past and ongoing colonial motivations. Government and health institutions must anticipate this overarching colonial context when making and communicating risk management decisions with Indigenous Peoples. In this vein, government authorities must work toward a praxis of decolonization in these relationships, including, for example, working in partnership with Indigenous nations to engage in collaborative risk mitigation and communication that meets the unique needs of Indigenous populations and limits the potential for less benign-though understandable-interpretations.

Dietary Intake Patterns and Lifestyle Behaviors of Pregnant Women Living in a Manitoba First Nations Community: Implications for Fetal Alcohol Spectrum Disorder.

The information on the nutrition status of women at-risk of carrying a child with fetal alcohol spectrum disorder (FASD) is scarce, particularly in the First Nations population living on reserve. This study examined and compared nutrition status, dietary intake, and lifestyle patterns of pregnant at-risk, defined as those who consume alcoholic drink during the current pregnancy, and non-at-risk women living in northern Manitoban community. Thirty-seven pregnant, First Nations women (at-risk n = 15; non-at-risk, n = 22) were recruited to participate in the study. A questionnaire, presented in paper and iPad formats, collected information on participants' demographics, dietary intake, lifestyle, pregnancy outcomes, and maternal health. A food frequency questionnaire and 24-h recall were used to determine nutrient intake. Nutrient values were assessed using Dietary Reference Intakes (DRI). At-risk and non-at-risk women were below the Canada Food Guide serving size recommended for Vegetable and Fruit, Grain, and Milk Products with 93%, 92%, and 93% of participants not meeting the recommendations, respectively. Women met the recommendations for vitamins A, B1, B12, C, niacin, choline, as well as calcium, and zinc. Sixty eight percentage (%) of participants did not meet the recommendations for folate and iron, and 97% for docosahexaenoic acid (DHA). Significant differences were observed between non-at-risk and at-risk women for mean % DRI intakes of vitamin C (313 ± 224 vs. 172 ± 81 mg/day), niacin (281 ± 123 vs. 198 ± 80 mg/day), folate (70 ± 38 vs. 10 ± 22 mcg/day), and iron (101 ± 74 vs. 74 ± 30 mg/day). The findings of this study lay a fundamental premise for the development of community nutrition programs, nutrition education, and nutrition intervention, such as community specific prenatal supplementation. These will assist in ensuring adequate maternal nutrient intake and benefit families and communities in Northern Manitoba with and without alcohol insult.

Thiamin deficiency on fetal brain development with and without prenatal alcohol exposure.

Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, γ-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD.

Genetic Variation in Human Vitamin C Transporter Genes in Common Complex Diseases.

Adequate plasma, cellular, and tissue vitamin C concentrations are required for maintaining optimal health through suppression of oxidative stress and optimizing functions of certain enzymes that require vitamin C as a cofactor. Polymorphisms in the vitamin C transporter genes, compromising genes encoding sodium-dependent ascorbate transport proteins, and also genes encoding facilitative transporters of dehydroascorbic acid, are associated with plasma and tissue cellular ascorbate status and hence cellular redox balance. This review summarizes our current knowledge of the links between variations in vitamin C transporter genes and common chronic diseases. We conclude that emerging genetic knowledge has a good likelihood of defining future personalized dietary recommendations and interventions; however, further validations through biological studies as well as controlled dietary trials are required to identify predictive and actionable genetic biomarkers. We further advocate the need to consider genetic variation of vitamin C transporters in future clinical and epidemiologic studies on common complex diseases.